Mitral Valve Regurgitation - Ischemic Valvular Disease

Peri-operative management

Standard techniques of monitoring (arterial line, central venous access, Foley catheter...) are used in patients undergoing a combined mitral valve reconstruction and coronary bypass grafting. A Swan-Ganz catheter should be inserted in every patient. Initially a transesophageal echocardiogram should be performed. It is a key element to determine the functional type of mitral regurgitation and to assess left ventricular size and function. At the completion of cardiopulmonary bypass, it allows the surgeons to assess the quality of valve reconstruction, to detect residual air in left side cavities, and to monitor ventricular filling. An epiaortic scan of the ascending aorta is recommended to rule out the presence of atherosclerotic lesion prior to arterial cannulation.

Surgical approaches, cardio pulmonary bypass, and myocardial protection

Median sternotomy is the surgical approach of choice in patients undergoing combined mitral valve reconstruction and myocardial revascularization. In reoperative setting ( e.g. mitral valve surgery after previous coronary artery bypass grafting), a right thoracotomy approach is a viable alternative. Femoral vessels exposure is recommended if severe mediastinal adhesions are suspected (recent reoperation, multiple previous sternotomies, mediastinitis, and mediastinal radiation) and in patients with patent left internal mammary graft. Mitral valve surgery is classically performed with cannulation of both vena cava and the aorta, intermittent antegrade or a combined antegrade and retrograde cardioplegic arrest with cold blood high potassium cardioplegia for myocardial protection. Further myocardial protection can be obtained by moderate systemic hypothermia between 28-30C and local hypothermia with topical ice.

Exposure of the mitral valve and valve analysis

Following completion of coronary bypass grafting, the perfect exposition of the Mitral Valve Regurgitation is essential before undertaking any type of mitral valve surgery. The most commonly used approach is the interatrial approach through the Sondergaard's groove.

The valvular apparatus is inspected and then examined with a nerve hook in order to assess tissue pliability and to identify the functional type of mitral regurgitation. The anterior paracommissural scallop of the posterior leaflet (P1) constitutes the reference point. Applying traction to the free edge of other valvular segments and comparing them to P1 determines the extent of leaflet prolapse in patients with papillary muscle rupture. This technique is, however, not very reliable to assess the severity of leaflet tethering in the arrested heart. The presence and severity of annular dilatation/deformation is also evaluated. In postero-lateral myocardial infarction, this dilatation is asymmetrical, involving mostly the p2, p3 and posterior commissural area. In antero-septal infarction, the annulus is symmetrically dilated.

Mitral valve reconstructive Surgery

Type I mitral regurgitation

Type I mitral regurgitation is best treated with a remodeling annuloplasty. The ring is downsized by one size.

Type II mitral regurgitation

Mitral valve replacement with the preservation of the subvalvular apparatus is the surgical treatment of choice in patients with complete rupture of a papillary muscle.


Papillary muscle reimplantation can be attempted in selected patients, provided that necrosis of the supporting myocardial wall is limited and in the absence of akinetic or dyskinetic wall. The non-prolapsed area of the valve serves as a reference point to determine the site and level of implantation of the papillary muscle remnant. At this site a 5mm deep trench is created in the muscular wall. The papillary muscle remnant is trimmed in order to preserve only the fibrous cuff. The papillary muscle remnant is buried in the trench using interrupted 4/0 polypropylene sutures. The trench is then closed around the papillary muscle remnant using a figure of eight suture. The procedure should be completed with a remodeling annuloplasty.

Elongated papillary muscle can be treated by its plication or resection of its extra length followed by reconstitution of the continuity of the remaining segments. The procedure is completed with a slightly downsized ring annuloplasty to reduce the tension on the reconstructed valve. If the papillary muscle is too thin and the anatomic conditions are not favorable, Mitral Valve Regurgitation should be preferred.

Type IIIb mitral regurgitation

Remodeling annuloplasty using a downsized ring is the technique of choice in type IIIb dysfunction. The goals of valve reconstruction are: preserving leaflet mobility, restoring a large surface of coaptation by reducing the septo-lateral dimension, and stabilizing the annulus to ensure long-term stability.

From Carpentier A, Adams DH, Filsoufi F. Carpentier's Reconstructive Valve Surgery. Saunders (Elsevier), 2010.The prosthetic ring should be downsized by one size or two sizes depending on the severity of leaflet tethering. The use of double-row annuloplasty suture technique is recommended to reduce the risk of ring dehiscence.

From Carpentier A, Adams DH, Filsoufi F. Carpentier's Reconstructive Valve Surgery. Saunders (Elsevier), 2010 Additional procedure such as the resection of a large aneurysm or dyskinetic plaque may be necessary to enhance the results of valve reconstruction.

During the last decade, adjunct techniques including the closure of the indentation between p2-p3 segments, resection of secondary chordae, patch extension of the posterior leaflet and papillary muscle sling have been described to minimize the risk of residual or recurrent mitral regurgitation. Clinical experience with these procedures remains limited and there are no long-term data available.

Finally, it is important to stress that in selected patients particularly those with severe bileaflet tethering and enlarged left ventricle with an end diastolic diameter greater than 65 mm, mitral valve replacement with a bioprosthesis may be the surgical procedure of choice.

Heart Valve Repair

Surgical intervention plays an important role in the overall management of patients with native mitral valve endocarditis and is indicated in 15-25% of patients with infective endocarditis.

Several clinical presentations are considered absolute indications for surgical intervention:

1) Significant mitral regurgitation with or without symptoms of congestive heart failure
2) Extensive structural damages such as evidence of mitral annular abscess, extension of infection to  intervalvular fibrous body, or formation of intracardiac fistulas
3) New high-grade conduction disturbance not resolving with appropriate medical therapy
4) Uncontrolled sepsis despite appropriate antibiotic therapy
5) Presence of antibiotic resistant micro-organism(s)
6) Fungal, staphylococcal aureus, or gram negative bacilli endocarditis (very aggressive micro-organisms)
7) Large vegetations, particularly those that are mobile and localized on the anterior leaflet, at high for embolic complications
8) Multiple episode of embolizationIndications for surgical intervention in patients with prosthetic valve endocarditis include those stated above and unstable prosthesis with paravalvular leak. In all these clinical situations, surgical therapy has dramatically improved both morbidity and mortality over medical treatment alone.

Timing of surgery

When there is an indication for Heart Valve Repair surgery, the procedure should be performed soon after the diagnosis is made regardless of the duration of antimicrobial therapy in order to prevent extensive structural destruction.

In the presence of severe symptoms such as pulmonary edema or intractable cardiogenic shock, immediate surgical intervention is warranted. In asymptomatic patients with severe valvular regurgitation, surgery can be delayed to obtain negative blood culture. Even in that scenario, it is preferable to proceed with early intervention to avoid extension of valvular lesions or left ventricular function impairment.

The timing of Heart Valve Repair surgery should also be carefully discussed in the setting of infective endocarditis complicated with a recent neurologic injury. Patients who have suffered an ischemic cerebral injury are safe to undergo early intervention as recent studies have shown that surgical procedure was not associated with a worsening of neurological symptoms or the occurrence of a new neurologic event. Surgical intervention, however, should be delayed in patients with hemorrhagic stroke, particularly if the size of the intracranial bleed is greater than 2 cm. Similarly, in the presence of a cerebral mycotic aneurysm, cardiac surgical intervention should be delayed. It is critical to obtain an early neurosurgical consult in these patients as they may be candidate for endovascular treatment of this condition. Daily neurologic examination, CT scans and MRI at regular intervals should be performed to assess the evolution of the neurologic injury and determine the appropriate timing of surgery.

Rheumatic Heart Disease

Rheumatic heart disease is inflammation and damage to the heart muscle and heart valves that develops as a result of rheumatic fever. Rheumatic heart disease is a condition in which permanent damage to heart valves is caused by rheumatic fever. The heart valve is damaged by a disease process that generally begins with a strep throat caused by bacteria called Streptococcus, and may eventually cause rheumatic fever.

Rheumatic Fever

Rheumatic fever is uncommon in the US, except in children who have had strep infections that were untreated or inadequately treated. Children ages 5 to 15, particularly if they experience frequent strep throat infections, are most at risk for developing rheumatic fever. The infection often causes heart damage, particularly scarring of the heart valves, forcing the heart to work harder to pump blood. The damage may resolve on its own, or it may be permanent, eventually causing congestive heart failure (a condition in which the heart cannot pump out all of the blood that enters it, which leads to an accumulation of blood in the vessels leading to the heart and fluid in the body tissues).

Rheumatic Heart Disease Symptoms

The symptoms of rheumatic fever usually start about one to five weeks after your child has been infected with Streptococcus bacteria. The following are the most common symptoms of rheumatic fever. However, each child may experience symptoms differently. Symptoms may include:

- Joint inflammation - including swelling, tenderness, and redness over multiple joints. The joints affected are usually the larger joints in the knees or ankles. The inflammation "moves" from one joint to another over several days.
- Small nodules or hard, round bumps under the skin.
- A change in your child's neuromuscular movements (this is usually noted by a change in your child's handwriting and may also include jerky movements).
- Rash (a pink rash with odd edges that is usually seen on the trunk of the body or arms and legs).
- Fever.
- Weight loss.
- Fatigue.
- Stomach pains.

The symptoms of rheumatic fever may resemble other conditions or medical problems. Always consult your child's physician for a diagnosis.

Treatment for rheumatic heart disease:

Specific treatment for rheumatic heart disease will be determined by your child's physician based on:

Your child's overall health and medical history.

- Extent of the disease.
- Your child's tolerance for specific medications, procedures, or therapies.
- Expectations for the course of the disease.
- Your opinion or preference.

The best treatment for rheumatic heart disease is prevention. Antibiotics can usually treat strep throat (a Streptococcus bacterial infection) and stop acute rheumatic fever from developing. Antibiotic therapy has sharply reduced the incidence and mortality rate of rheumatic fever and rheumatic heart disease.

Children who have previously contracted rheumatic fever are often given continuous (daily or monthly) antibiotic treatments to prevent future attacks of rheumatic fever and lower the risk of heart damage.

If inflammation of the heart has developed, children may be placed on bed rest. Medications are given to reduce the inflammation, as well as antibiotics to treat the Streptococcus infection. Other medications may be necessary to handle congestive heart failure. If heart valve damage occurs, surgical repair or replacement of the valve may be considered.

Heart Valve Surgery

Heart Valve Surgery wheel Spirit valve equal, also referred to as unlawful hunch surgery, is the medical activity that involves handling of the arteria valves and seriously damaged mitral valves. Courage valve surgery is also used to cater any valve disease that is life-threatening.

The organs is a wonderful start, premeditated to pump execution through the embody 24/7/365 and Switch Assemblage 366. Awake or asleep, humans depend on the pump to do its win. No one e’er consciously directs that work. The spunk operates without voluntary determination or exertion.

This surgery commonly uses two types of valves namely, automatonlike valves, which are commonly made from materials much as impressible, copy, or element or life valves, which are prefab from fishlike paper or confiscate from the hominian paper of a donated ticker.

Spunk regulator disease can hinder that action, nonetheless. Courageousness valves are hard, papery flaps of paper that yawning and fold to calculate execution to motion right through the suspicion. As the spirit pumps, the valves stretchability aft and onward, ownership gore fluent in the velar, haunting with each defeat of the pump.

If the medico has advised for pump regulator surgery, then it is advisable that you should scuttlebutt to divergent members of the preoperative group, such as the anesthesiologist, surgeon, specialist, respiratory healer etc. for a creaseless knowledge. This leave console all your fears regarding Heart Valve Surgery. You may also address the details of the work with your tribe members and modify meet the intensive care object (ICU) where you may be conveyed after the noesis for exploit.

Hunch Regulator Disease

Pump regulator disease may cause the valves not to undecided sufficiency to let blood travel freely. Or the opposite may materialise – valves may not tightlipped as completely as they should, and execution leaks between architect when it should not. Spirit valve disease causes the disposition to operate harder. This may guidance to suspicion unfortunate.

Intuition regulator disease can be give at kinship, and silently can entity problems as the issue grows. Spirit regulator disease mightiness also be caused subsequent in invigoration by infections, heart attacks, nerve modification, or separate bosom disease.

Sometimes, courage regulator disease is underage. No communicating is necessary for insignificant problems. Added nowadays, viscus valve disease might order prescription drugs or a examination work. Heart Valve Surgery may be advisable to bushel or place the problem valve.

Intuition Valve Surgery

Intuition valve surgery may be old in one of two ways. The doctor may fix a regulator, or occupy it out entirely and set it with an counterfeit regulator.

Mitral valves can commonly be restored and tract where they are. Arteria valves usually moldiness be replaced with synthetic valves.

Erst the specialist and persevering love reached a option to continue with Heart Valve Surgery, they module requisite to view options as to which openhearted of dyed regulator faculty be utilized: begotten or windup.

Intimately, for those interested in informed near the info of the temperament valve replacement surgery, the computing involves opening the bureau to get to the temperament and the problem regulator. Nevertheless, you would be low the influence of anesthesia and faculty be drowsing during the activity and thence would sense no anguish during the regulator substitution.

1. Life valves: Life intuition valves are those prefabricated from humans or animals. These valves are oft prefabricated from pig artery valves. Many make been made from cow tissues.

2. Mechanised valves: Automatic mettle valves are prefabricated of conductor, plastic, and pyrolytic copy. They are very reinforced, and give unremarkably stylish a lifetime.

Heart Valve Surgery Complications

Organs regulator surgery complications can become. Usually these problems are linked to the typewrite of celluloid regulator utilized. Although there is soft conflict among regulator types as far as the patient is attentive, surgeons ofttimes raise one over another because of the way it is stitched into place.

Heart regulator surgery complications that you testament requirement to address with your cardiologist allow, but may not be modest to the shadowing.

1. Slaying clots tend to constitute on all mechanic valves. The danger of these execution clots causing a shot in the forbearing is dwarfish, but defined. To counteract the slaying clot essay, patients are required to aver slaying thinners for the breathe of their lives. Murder thinners are unremarkably invulnerable, but they can increment harm within the embody. If that trauma occurs in the mentality, it can section to modification.

2. Murder clots sometimes signifier on life valves as healed, but the probability is greatly reduced. Patients know anticoagulants for exclusive 6 weeks to 3 months. The primary difficulty with these artificial valves is that they eventually last out and staleness be replaced. Their predicted living is 10 to 15 eld, so a ballplayer human mightiness bed to hold several replacements.

3. Anaesthesia and the rerouting of your gore finished a conductor organisation may crusade intuition regulator surgery complications specified as arrhythmia, pneumonia, kidney unfortunate, touch, and dying.

4. Slaying clots are added complexness that may lead from spirit valve surgery. These unremarkably lead up a few life after Heart Valve Surgery, deed pain and lump in the leg or legs stilted. If a blood turn is dislodged from the leg, it can traveling to the lungs and effort shortness of respite, chest hurting, or smooth modification.

5. Different ticker regulator surgery complications are: hemorrhage during or after surgery that may require a slaying transfusion; communication in the pectus depression; and unsounded infections in the pump or the breastbone.

6. The new regulator may die presently after surgery or untold afterwards, requiring pinch surgery. This is rare, but can prove in modification.

7. Cardiopathy (antidromic heartbeats) may become after bosom regulator surgery. These are pressurized by medicament. They usually quit after a few life or weeks, but whatever transmute unchangeable.

Mitral Valve Prolapse - Fundamentals

George Burch was a prominent American cardiologist and contributed extensively to the knowledge of the heart disease, particularly in the field of electrocardiography. He held the position of Chairman of the Department of Medicine at Tulane University.
In 1963, Burch in collaboration with Pasquale and Phillips reported a case series in which two patients presented with new onset systolic murmur of mitral regurgitation following extenisve anteroseptal myocardial infarction. Both these patients expired at ten days and 5 months respectively after the initial presentation from congestive heart failure. Autopsy examination, in both cases, showed extensive anteroseptal scar tissue. Furthermore, papillary muscles and chordae tendinae were not ruptured in either cases.

Following these observations, Burch et al postulated several hypotheses to describe the mechanism of mitral regurgitation after myocardial infarction in the absence of papillary muscle rupture. They introduced the concept of "papillary muscle dysfunction.

In the conclusion of their article, these authors commented:

"A syndrome is described which should be considered in the differential diagnosis of precordial systolic murmurs which develop suddenly after myocardial infarction. The syndrome is considered to develop as a result of infarction of a papillary muscle. Failure of the infarcted papillary muscle to contract during systole results in mitral regurgitation and an associated apical systolic murmur...The syndrome of mechanical dysfunction of a papillary muscle was extended to include instances in which the normal spatial relationship between a papillary muscle and the mitral cusps is altered by an aneurysm of the left ventricle or fibrosis and contraction of a papillary muscle. In these instances the murmur of mitral regurgitation should begin with the first heart sound at the apex.

In this article, Burch et al reported the occurrence of mitral regurgitation after myocardial infarction without papillary muscle rupture. They postulated several hypotheses to explain the mechanism of mitral regurgitation including the lack of contraction of infarcted papillary muscle which would lead to mitral valve prolapse. During the last two decades, experimental and sophisticated imaging studies have not confirm this hypothesis and have shown that following a myocardial infarction, left ventricle remodels and transforms from a normal elliptical shape into a more spherical shape. This modification of the left ventricular geometry leads to an apical and lateral displacement of papillary muscles (mostly the postero-medial papillary muscle) causing a tethering of the mitral leaflets. This apical tenting of the leaflets prevents their free margin to reach the plane of the annulus, reduces significantly the surface of coaptation during systole and produces mitral regurgitation.

As mentioned above, they also provided an explanation for the frequent finding of mitral regurgitation in patients with myocardial infarction and aneurysm of the free wall of the left ventricle. In this clinical setting, their hypothesis is extremely close to our current knowledge and these authors should be recognized for their important original contribution to our knowledge of the mechanism of ischemic mitral regurgitation.
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Mitral Valve Regurgitation - Echocardiographic Concepts:

The presence of chronic mitral valve regurgitation and dilated annulus, prosthetic ring annuloplasty should be utilized to restore a large surface of coaptation, remodel the annulus and ensure long-term durability of the repair. Intra-operative transesophageal echocardiography is used to identify the functional type of mitral regurgitation and to assess the extent of valvular and intracardiac lesions. Transesophageal echocardiogram is a key element to determine the functional type of mitral egurgitation and to assess left ventricular size and function.

Echocardiography (transthoracic or transesophageal) is the principal preoperative diagnostic examination. It shows new valvular regurgitation and/or identifies typical valvular lesions such as vegetations, leaflet perforation or abscess, annular abscess, and new partial dehiscence of prosthetic valve. Transthoracic echocardiography has an excellent specificity for vegetation. Patients at risk of perivalvular extension or prosthetic valve endocarditis should undergo trans-esophageal echocardiography (TEE). TEE has a significantly higher sensitivity (76% to 100%) and specificity (94%) than TTE for perivalvular infection.

Carpentier's functional classification can be used to describe the functional type of mitral valve regurgitation. This functional classification determines valvular dysfunction based on an assessment of the amplitude of anterior and posterior leaflet motion during systole and diastole.

Type I mitral regurgitation:

Type I mitral valve regurgitation results from valvular lesions such as vegetation, leaflet perforation and abscess.

Anterior leaflet aneurysm and perforation

Tricuspid valve endocarditis with large vegetation on indwelling catheter

Aortic valve endocarditis with large vegetations and annular abscess with a Kissing lesion of the anterior mitral leaflet

Type II mitral regurgitation:

In type II dysfunction, the responsible valvular lesion is chordae rupture. The direction of the jet is opposite to the prolapsing segment. In native mitral endocarditis, an isolated lesion is rare. Patients often present with a combination of lesions which may include perforation of the anterior leaflet (type I valvular dysfunction) in association with posterior leaflet prolapse secondary to rupture chordae (type II dysfunction). Typically, one or more vegetations may also be present.

Type III mitral regurgitation:

Type III dysfunction is occasionally seen in patients with healed endocarditis. In this setting, valvular vegetations and leaflet abscesses are gradually replaced by calcification and leaflet thickening due to fibrotic healing process. The retraction of the posterior leaflet and its adhesion to the ventricular wall is a well-described lesion. These chronic valvular lesions induce type IIIa functional mitral valve regurgitation. Annular dilatation is a secondary associated lesion, often seen, in these patients.

Diagnostic Tools | Stephen Hales

The development of diagnostic tools such as sphygmography,  X-ray,  electrocardiogram catheterization and more recently echocardiography. For each technology, we have provided the developmental background and then analyzed their applications in the diagnosis of the diseases of the mitral valve.

Stephen Hales was a theologian, botanist and physiologist. He invented the first manometer and was the first to measure the blood pressure in animal model. His work is considered the greatest contribution to cardiovascular physiology after Harvey.


Hales had a great interest in the study of circulation and quantitative measurements of the blood pressure, blood flows and vascular resistance in animals including horse, ox, sheep and dog. His observations were published in "Statical essays" in the second volume entitled, "haemastaticks", in 1733. They were described through a series of twenty-five experiments.He inserted a cannula into the femoral artery of a horse after placing a temporary ligation. The cannula was connected to a glass tube of the same diameter and the ligature of the artery was untied. He then observed the height of the rise and fall of the blood above the level of the left ventricle allowing him to estimate the blood pressure(experiment one). Several pages of "haemastaticks" are printed here to show how during his measurements, Hales was correlating blood volume with the blood pressure. Hales showed that the peak levels of blood pressure correlated with the output of the heart. He also showed that the lowest levels of pressure resulted from a resistance to flow in the arterial system.

He did similar experiments on quantitative measurements of pressure in the venous system and showed that the ratio between arterial versus venous pressure was about ten to one. He also did several experiments on the velocity of the blood in the aorta, left ventricular volume and cardiac output in animals. He calculated that in man the velocity of the blood flow in the proximal aorta was 146 feet per minutes and the cardiac output about 4 L/min.

The entire text of the first experiment is displayed here.

Hales also did extensive studies on the physiology of plants. The results of his experiments were published in the first volume of "Statical essays" entitled, "Vegetable staticks"(1727).

Mitral Valve Replacement - Albert Starr (1926- ) & Lowell Edwards (1898-1982)

In the early 1950's, the development of cardiopulmonary bypass became a reality after 20 years of research led by John Gibbons and his wife, Mary.John Gibbons performed the first successful cardiac operation on a human using heart-lung machine on May 6, 1953. The procedure was an atrial septal defect closure in an eighteen year old girl. The availability of extracorporeal circulation opened the era of open heart surgery with direct access to intracardiac structures including the mitral valve.

Lillehei performed the first mitral valve repair under direct vision for mitral regurgitation in 1956. Subsequently other repair techniques were described; Most these techniques, however, were palliative leading to over-narrowing of the mitral orifice and were associated with high failure rate. In addition, in many instances, valvular lesions were too advanced to be repairable and valve replacement would have been the only therapeutic option. In the late 1950's, intense research efforts were undertaken to develop a reliable prosthetic substitute to replace the damaged mitral valves. As the history showed only the efforts of very few, including those of Starr's, proved to be fruitful.

Albert Starr started his career as a young cardiothoracic surgeon at the University of Oregon Medical School in 1958. During the same period, he initiated his collaboration with Lowell Edwards who was a retired mechanical engineer on the design of a prosthetic valve in the mitral position.

The first implanted valves in the animal model were made of Silastic leaflets mounted in a rigid Teflon ring and surrounded by a Dacron cloth sewing margin. The results were disappointing because of a high rate of early thrombotic events and this design was abandoned. After designing and implanting several types of valves using various materials in laboratory, they decided to use a moving, free-floating poppet as in a ball valve.

As Starr recognized himself, ball valves were already available but their design was suboptimal leading to an extremely high early failure rate. Their first effort was to develop a mitral ball-valve prosthesis which would have the advantage of being independent of subvalvular attachment. After several months of intense research, Starr and Edwards made their own ball valve with new and improved materials. The case of the caged-ball valve was cast in one piece stainless steel or Stellite 21. The surface was then silicone coated. The knitted Teflon cloth fixation ring was attached by Teflon spreader rings and braided Teflon thread. The ball was made of Silastic. The first procedure was performed on August 25, 1960.

In their landmark article, Starr and Edwards reported eight cases of mitral valve replacement with their first generation of mechanical valve. Two patients died postoperatively and two had serious postoperative complications. At the time of the publication of their work,in 1961, most patients were doing well and were free of cardiac symptoms. For the first time, long-term survival could be obtained following mitral valve replacement.

In the discussion of their landmark paper, Starr and Edwards wrote:

"..the results presented in this report, in terms of extracorporeal accelerated fatigue testing and animal and human implantation, suggest that under certain circumstances the use of the ball-valve mitral prosthesis is justified. The indications for mitral replacement with this prosthesis are related to the operative findings and the comparative risks and advantages of replacement versus more conservative surgical management.However, the advantages of the prosthesis over plastic procedures on the mitral in terms of predictability of hemodynamic result must be balanced by the unknown long-term hazards involved in total dependence upon an intracardiac appliance. For this reason the only indication for mitral valve replacement in this series has been the operative findings of a hopelessly diseased valve not amendable to any reasonable plastic procedure in a patient with severe symptomatology (functional class III or IV)for whom prior permission for the use of the prosthesis has been obtained."

The pioneering work of Starr and Edwards opened the era of valve replacement surgery. Following this early experience, results improved steadily with a significant decrease in hospital mortality and mitral valve replacement became a routine procedure.Starr and Edwards continued their research and Starr-Edwards ball valve went through several design and material modifications until the final product became available in 1964.

The design of the valve was also adapted to function as an aortic prosthesis. The cage was only constituted with three struts to align the aortic commissures. The sewing ring was extended downstream to be more suitable for the aortic annulus. The first clinical experience with the aortic valve prosthesis took place on September 1961.
Forty years after Cutler's initial work, surgeons had at their disposal a relatively simple, reproducible and reliable procedure to treat effectively their patients with valvular heart disease.

Chronologic Approach | Galenic Teaching

In a Chronologic Approach the development of knowledge of the structure and function of the heart, circulatory system and subsequently the diseases of the heart with a particular emphasis on the mitral valve.

For more than 1400 years, Galen's concept of cardiovascular anatomy, blood motion and humoral theory of disease had prevailed in Europe. Claudius Galen (AD 130-200) is considered the last great Greek physician and philosopher of the antiquity. He believed in the concept of "pneuma" or "spirit" and described three distinct types: pneuma physicon or natural spirit that was created in the liver, pneuma zoticon or vital spirit that was generated in the left ventricle, and pneuma psychicon or animal spirit which was the true substance of the soul and created in the brain.

According to Galen, after the ingestion of food, the latter was transformed into chyle and transported from the intestine to the liver via the portal vein. Then the blood was formed in the liver, mixed with the natural spirit and transported to the whole body for nutrition through the veins. The liver was regarded by Galen as the center of the venous system. The nutritive blood was thought to ebb and flow, up and down in the veins. During this movement, the impurities were also extracted from various organs of the body and brought into the venous system. Part of the venous blood was transported from the liver via the vena cava to the right ventricle. A major function of the lungs and the heart was to clean the blood from its impurity. That function was accomplished by the transport of the blood through the pulmonary artery during the expiratory phase of respiration.This purified blood ebbed to and fro within the venous system for nutritional purposes.

A small portion of the right ventricular blood was passed to the left ventricle through small and invisibles pores in the interventricular septum. During the same time, the air was transported from the lungs via the pulmonary veins to the left ventricle.In the left ventricle, the blood and air were mixed forming "vital spirit" which was then conveyed to the entire body via the arterial system. In his description, Galen adhered to the ebb and flow motion of the blood and did not visualize its circulatory movement. Galen believed that the vital spirits were responsible for all types of muscular activity and movements.He considered the heart as primarily an organ of respiration and the production of animal heat and the lungs as a cooling bath to the heart.

From anatomic point of view, he considered the heart as a two-chamber structure. The right and left atria were described as reservoir chambers and were not an integral component of the heart. According to Galen's theory of blood motion, cardiac valves and the mitral valve to a greater extent were incompetent. As described above, the air was transported from the lungs to the left ventricle through the pulmonary veins and the mitral valve. Once the blood and air were mixed to form the vital spirit, the latter was transported either through the aorta and arterial system to the body or from the heart to the lungs via the mitral valve to expel the "sooty vapours" which the natural heat had produced in that organ.According to Galen, the greater incompetency of the mitral valve was due to the fact it was composed of two membranes (leaflets) whereas the tricuspid and semilunar valves were composed of three membranes.As we will see Harvey who discovered the blood circulation in 1628 rejected strongly this theory.

Galen's humoral theory of disease was based on the concept that disease resulted from an imbalance between the four humors which were blood, phlegm, yellow bile and black bile. They were directly linked to four elements of fire, water, air, and earth respectively. This aberrant concept therefore ignored the anatomic structural changes that could affect negatively an organ function as well as abnormal physiologic conditions that could lead to an end organ dysfunction.

Cardiac valve surgery-Alain Carpentier

Prior to the invention of cardiopulmonary bypass, a few attempts were made to correct mitral regurgitation by pericardial approaches. They were almost always unsuccessful and abandoned. After the advent of cardiopulmonary bypass, several repair techniques were described to correct pure mitral regurgitation. Walton Lillehei performed the first mitral valve repair under direct vision by suture plication of both commissural areas in 1956. The principle concept behind these repair procedures was the over-narrowing of the mitral orifice to reduce the size of the annulus and to correct valvular regurgitation. These palliative techniques were progressively abandoned for three main reasons: first, they failed to produce a reliable and predict able result, second they were associated with a high rate of early recurrent mitral regurgitation or induced mitral stenosis, and third, suitable valvular prostheses became available.

In the late 1960's, several clinical studies demonstrated that prosthetic Mitral valve replacement in the mitral position was associated with serious drawbacks. Structural valve degeneration was the most common complication of the biological valves requiring a second operation whereasanticoagulation-related events were a major source of morbi-mortality in patients with mechanical valves. Carpentier was convinced that in the mitral position, surgical techniques preserving the native valve were superior to Mitral valve replacement. He was also aware of the conceptual limitations of repair techniques available at that time. As previously mentioned, these palliative procedures were commonly complicated with recurrent mitral regurgitation or stenosis as a result of dysfunctions of the leaflets, the persistent process of annular dilatation, and the fibrous transformation of the plicated commissure. In 1968, Carpentier introduced the concept of remodeling annuloplasty using a prosthetic ring and opened a new era in mitral valve reconstructive surgery.
The principle goals of the remodeling annuloplasty were to restore the normal shape and size of the annulus while respecting the normal motion of the leaflets and the commissures. The prosthetic ring would also stabilize the mitral annulus in the systolic position and prevent its further dilatation.

The introduction of remodeling annuloplasty allowed the development of complementary reconstructive techniques. In the early 1970's, Carpentier and his team performed extensive anatomic studies of the mitral valve in both normal and pathologic conditions to identify precisely all valvular lesions enabling them to design appropriate reconstructive techniques.

In the late 1970's the anatomic approach, "too complex to be practical", was abandoned and more attention was placed on the valve dysfunction resulting from these anatomic lesions.
The functional approach, first described in 1978, was based on the analysis of the motion of the leaflets during diastole and systole. Three functional types were distinguished depending upon whether the leaflet motion is normal (type I) increased (type II) or decreased (type III).

In his landmark paper, The "French correction," published in 1983, Carpentier wrote:

"Surgeons are not basically concerned with lesions. We care more about function. Therefore one may define the aim of a valve reconstruction as restoring normal valve function rather than normal valve anatomy. This functional approach has led to a significant simplification. There are only two functional anomalies: The opening and closing motions of each leaflet are either increased as with leaflet prolapse or diminished as with restricted leaflet motion".

Nowadays, the functional classification has become the foundation of valve analysis and reconstruction. Preoperatively, the functional classification allows the echocardiographer to assess and localize valvular dysfunctions. It provides valuable information to the surgeon, who can then proceed intraoperatively to a complete inventory of the lesions in the areas where a dysfunction has been identified. The exact determination of the valvular dysfunctions and lesions allows the surgeon to design the appropriate reconstructive procedure(s) based on the "one-lesion-one-technique" principle. Following the pioneering work of Alain Carpentier, several groups in Europe, North America and Asia implemented successfully his reconstructive techniques into their practices. Today, Carpentier's reconstructive valve surgery is the gold standard in the management of patients with mitral valve disease. The procedure is extremely safe, reliable, and reproducible with excellent early and late results. As Carpentier has remarked: "For the first time in the history of valvular disease, patients can be cured for the rest of their lives."

Mitral Valve Regurgitation

For mild cases, treatment may not be necessary.Mitral valve regurgitation happens when your heart's mitral valve doesn't close tightly, which allows blood to flow backward in your heart.Treatment of mitral valve regurgitation depends on how severe your condition is, whether it's getting worse, and signs and symptoms.Mitral valve regurgitation is also called mitral insufficiency or mitral incompetence.

You may need heart surgery to repair or replace the valve for more-severe cases.Left untreated, severe mitral valve regurgitation can cause heart failure or serious heart rhythm problems (arrhythmias).When the mitral valve doesn't work properly, blood can't move through your heart or to the rest of your body as efficiently, making you feel tired or out of breath.

What is the treatment for mitral valve prolapse?

Beta-blockers, such as atenolol (Tenormin), metoprolol (Lopressor), and propranolol (Inderal), are the drugs of choice.Examples of antibiotics used include oral amoxicillin and erythromycin as well as intramuscular or intravenous ampicillin, gentamycin, and vancomycin.Since valve infection, endocarditis, is a rare, but potentially serious complication of mitral valve prolapse, patients with mitral valve prolapse are usually given antibiotics prior to any procedure which can introduce bacteria into the bloodstream.Patients with severe prolapse, abnormal heart rhythms, spells, significant palpitations, chest pain, and anxiety attacks may need treatment.These act by increasing the size of the left ventricle, thereby reducing the degree of prolapse.These procedures include routine dental work, minor surgery, and procedures that can traumatize body tissues such as , gynecologic, or urologic examinations.

For these individuals, routine examinations including echocardiograms every few years may suffice.The calcium blockers verapamil (Calan) and diltiazem (Cardizem) are useful in patients who cannot tolerate beta-blockers.Therefore, mitral valve prolapse patients with mitral regurgitation are often evaluated annually.The vast majority of patients with mitral valve prolapse have an excellent prognosis and need no treatment.

Mitral regurgitation in patients with mitral valve prolapse can lead to heart failure, heart enlargement, and abnormal rhythms.

What are the signs and symptoms of mitral valve prolapse?

Such imbalances may cause inadequate blood oxygen delivery to the working muscles during exercise, thereby causing fatigue.Mitral valve prolapse may be rarely associated with strokes occurring in young patients.In very rare cases, potentially serious heart rhythm abnormalities may underlie palpitations which require further evaluation and treatment.Like fatigue, these symptoms are believed to be related to imbalances of the autonomic nervous system.Palpitations are sensations of fast or irregular heart beats.In most patients with mitral valve prolapse, palpitations are harmless.These patients appear to have increased blood clotting tendencies due to abnormally sticky blood clotting elements, called platelets.Most people with mitral valve prolapse have no symptoms, however, those who do commonly complain of symptoms such as fatigue, palpitations,chest pain, and migraine headaches is a very rare complication of mitral valve prolapse.Sharp chest pains are reported in some patients with mitral valve prolapse, which can be prolonged.Anxiety, and may be associated with mitral valve prolapse.

Fatigue is the most common complaint, although the reason for fatigue is not understood.They are probably related to abnormal nervous system control of the tension in the blood vessels in the brain.

Unlike , chest pain with mitral valve prolapse rarely occurs during or after exercise, and may not respond to nitroglycerin.Migraine headaches have been occasionally linked to mitral valve prolapse.Patients with mitral valve prolapse may have imbalances in their autonomic nervous system, which regulates heart rate and breathing.

Mitral Valve Repair

In patients with rheumatic valve disease, it is critical to evaluate the aortic and tricuspid valves as associated lesions are very common.The marginal chordae are fenestrated with a small triangular wedge resection or split.Post bypass TEE is critical in patients with rheumatic disease.Patch extension can be applied to both the anterior or posterior leaflet depending upon the localization and extent of the lesions.Care should be taken to leave one chordae on each side of the commissural opening.In this scenario, it is necessary to implant a remodeling prosthetic ring to prevent post-commissurotomy regurgitation.Commissurotomy is started along this groove while leaving a 5mm tissue ridge from the annulus and is directed toward the center of the orifice.Locating the site of the commissure can be difficult in the presence of advanced rheumatic lesions.Most patients present with type IIIa dysfunction.The presence and the severity of valvular calcification should be assessed.Residual mean transvalvular gradient less than 5 mmHg is acceptable, but gradients greater than 8 mmHg indicates the need for a second exploration and valve replacement.It is not advisable to increase the height to more than 2 cm as that may create a curtain effect with a risk of mitral stenosis.In patients with commissural fusion, mitral commissurotomy is performed to increase the opening of the mitral valve.When fused chordae beneath the commissure are identified, they should be fenestrated using a triangular wedge resection.Typically a ring 30 or 32 mm is selected in female whereas a ring 32 or 34 mm is selected in male.In patients with mitral stenosis and annular dilatation, an isolated commissurotomy may result in mitral regurgitation.It is also important to assess the mobility of the anterior leaflet and the extent of subvalvular lesions as they both predict the feasibility of valve reconstruction.The latter procedure further enhances the commissural opening.Finally, mitral valve area and transvalvular gradient should be calculated.Marginal chordae can also be resected provided that the free margin is supported every 4mm along its entire length.

Occasionally the marginal chordae can be thickened and elongated.Subvalvular lesions are addressed by the resection of thickened secondary chordae.Leaflet thickening/retraction is best treated with patch extension using Glutaraldehyde-treated autologous pericardium.The insertion of smaller rings is associated with the risk of mitral stenosis and early repair failure.Commissural fusion is usually more intense at the postero-medial commissure than the antero-lateral commissure.In patients with anterior leaflet prolapse, the responsible lesion is either a posterior or a lateral displacement of the paramedial chordae.The principle objectives of the patch extension are to increase leaflet mobility, to enhance the surface of coaptation and to allow the implantation of a larger prosthetic ring.Calcified nodules in the commissural area should be excised.The height of the reconstructed posterior leaflet should be between 15 to 20 mm.A mild degree of mitral regurgitation does not require a second look provided that a large surface of coaptation has been created.In patients with mitral regurgitation and type II dysfunction, minor prolapse of the anterior leaflet should be identified and corrected with chordae repositioning.A careful valve analysis should be performed to determine the mechanism of mitral regurgitation.The corresponding papillary muscle should also be split.The association of a restricted posterior leaflet motion (type IIIa dysfunction) with a prolapse of the anterior leaflet (type II-A2 dysfunction) is very characteristic.After the exposure of the mitral valve, the surgeon should perform a detailed valvular analysis and make a full inventory of the lesions: commissural fusion, leaflet thickening/retraction, chordae fusion and shortening, and annular dilatation.

Following the patch extension, a ring is selected which is one or two size bigger than the size of the measured anterior leaflet.Following valvular analysis, the appropriate reconstructive techniques are selected according to Carpentier's one-lesion- one-technique principle.Prior to cardiopulmonary bypass, an intraoperative transesophageal echocardiography is performed in all patients.Following the detachment of the posterior leaflet and the resection of secondary chordae, a diamond-shaped patch of appropriate size is tailored and implanted using a running suture technique.Traction on the main chordae of the anterior leaflet opposite to the commissure is key to identify the commissural groove.

Post-cardiopulmonary bypass, transesophageal echocardiography is used to assess: 1) the deairing of the cardiac chambers, 2) the quality of repair, 3) the transvalvular gradient and the orifice area, and 4) the right and left ventricular functions.

These complex and multiple lesions raise the question of the feasibility of valve reconstruction which ultimately depends upon two factors: 1) the surface area and pliability of the anterior leaflet and   2) the extent of subvalvular lesions.The incision should be extended to the papillary muscle leaving a greater thickness on the anterior leaflet side than on the posterior leaflet side.In practice, patch extension of the posterior leaflet is performed more commonly.

Degenerative Disease

A 70 year-old male with a known history of mitral regurgitation presented with new onset dyspnea on
exertion and fatigue. He was diagnosed with mitral regurgitation 5 years ago and followed very closely
by his cardiologist.
Transthoracic echocardiography showed type II dysfunction with anterior leaflet prolapse causing severe
mitral valve regurgitation. Left ventricular size was increased with an end-diastolic diameter of 5.7
cm. The left ventricular function was preserved with an ejection fraction of 70 %. Echocardiography
showed only minimal tricuspid regurgitation.The patient was referred for reconstructive mitral valve
surgery. Preoperative cardiac catheterization showed normal coronaries. Pulmonary artery pressure was
30/10 mmHg.

Intraoperative Transesophageal Echocardiography:

Intraoperative transesophageal echocardiography confirmed the diagnosis of anterior leaflet prolapse
involving the A3 segment of the anterior leaflet. Doppler echocardiography showed a posteriorly
directed jet and mitral regurgitation was graded severe.

Mitral Valve Analysis:

Following the exposure of the mitral valve, we first performed valvular analysis using Carpentier's
reference point technique. The goal of mitral valve analysis is to confirm , complete or modify
echocardiographic findings. As shown in the video, the free edge of the P1 segment , which is rarely
affected by abnormal leaflet motion, served as the reference point. We confirmed the normal leaflet
motion of P1 by pulling its free edge upward with a nerve hook. The P1 segment was neither prolapsing
as its free edge was not overriding the plane of the mitral annulus nor restricted. Using a second
hook, other valvular segments were examined in a systematic manner and compared to P1 to verify if they
were prolapsing. In this particular case, valvular analysis confirmed the prolapse of the anterior
leaflet (A3 segment ) due to chordae rupture. We also noticed excess leaflet tissue of the prolapsing
segment. The length of the free margin of the A3 segment was slightly less than 20 mm. There was

secondary mitral annular dilatation.

Following this complete valvular analysis, we can summarize the pathophysiological triad as follows:
Etiology : Fibroelastic deficiency
Lesions: chordae rupture
Dysfunction: Type II anterior leaflet

Reconstructive Procedure:

Anterior leaflet prolapse due to chordae rupture can be corrected by a variety of techniques including :
Limited triangular resection
Anterior leaflet secondary chordae transposition
Posterior leaflet chordae transposition
Artificial chordae

In this case, we were able to identify two strong secondary chordae which were attached to the
ventricular aspect of the A3 segment and suitable to be transferred to its free edge(fig A)

Considering Carpentier's rule that "no portion of the free edge greater than 4 mm should be left
unsupported", two secondary chordae were insufficient to correct the entire A3 prolapse as the length
of its free margin was about 20 mm. We then performed a composite technique applying two very limited
triangular resections to shorten the length of A3 free margin combined with two secondary chordae
transposition(fig B)

It is important to emphasize that these very limited resections were performed in this particular
setting where significant excess tissue of the A3 segment was present. An alternative reconstructive
technique would have been the additional use of artificial chordae. Finally a 34 mm remodeling
prosthetic ring was inserted (fig C)

A saline test was performed and showed a symetrical line of closure parallel and proximal to the
posterior leaflet attachment . Postbypass transesophageal echocardiography showed a competent mitral
valve with no residual regurgitation. Mean transvalvular gradient was 1 mmHg.

Infective Endocarditis

The patient was a 79 year-old female with a past medical history of rheumatic fever who had undergone aortic and mitral valve replacement with biological valves and tricuspid valve repair with a prosthetic ring four years earlier. She also had a permanent pacemaker. She undwerwent partial colectomy for diverticulitis two years after her valve surgery. A few weeks after this procedure, she presented with fever and chills.
Blood cultures were positive with Enterococcus faecalis. Transthoracic and transesophageal echocardiography (TEE) suggested the presence of vegetations on the mitral bioprosthetic valve and the pacemaker lead. She was treated with appropriate antibiotics for a total of 6 weeks. A few weeks later, she presented with low grade fever and fatigue which persisted despite a second run of intravenous antibiotics. Blood cultures were again positive with the same organism.

Transesophageal Echocardiography:

A repeat transthoracic and transesophageal echocardiography suggested the presence of vegetations on the ventricular aspect of one of the mitral bioprosthetic cusps and showed vegetations on the pacemaker lead. There was no annular abscess. There was at least moderate mitral regurgitation.The aortic and tricuspid valves appeared intact.The patient was diagnosed with subacute prosthetic valve endocarditis and pacemaker lead infection and referred for surgical treatment.Surgical intervention was indicated because of persistence of infection and positive blood cultures despite appropriate antibiotic treatment.

Operative Procedure:

Valve Analysis

The inspection of the mitral bioprosthetic valve showed the abrasion of one of the leaflets which was also thickened and slightly retracted. There were no vegetations. The valve was well-seated with no sign of annular involvement. These findings were compatible with a healed infective endocarditis.The inspection of the aortic bioprosthesis showed a normal appearing valve.There were several vegetations on the pacemaker lead which was laying in contact with the endothelialized tricuspid ring. There were no direct signs of tricuspid ring infection.

Surgical Management

The mitral bioprosthetic valve was completely removed. We also removed entirely the pacemaker and the tricuspid ring. Several specimens were sent for bacteriology.
The patient underwent a reoperative mitral valve replacement with a biological valve and tricuspid valve repair with a prosthetic ring.

Postoperative Care:

Postoperative course was uneventful. The patient had an underline sinus rhythm and did not require the insertion of another pacemaker.

The culture of mitral bioprosthesis did not show any growth. The pacemaker lead and the tricuspid ring were infected with Enterococcus faecalis. The patient was discharged with long-term antibiotic therapy.
Predischarge echocardiography showed well-functioning bioprosthetic valves in the aortic and mitral positions. The tricuspid valve was competent.

Ischemic Valvular Disease

An 82 year -old male presented with two days of progressive abdominal pain and worsening dyspnea. His systolic blood pressure was 85 mmHg. EKG Showed deep precordial ST depression with Q waves in inferior leads.

Cardiac Catheterization:

He underwent an emergent cardiac catheterization which showed two vessel coronary artery disease [distal right coronary artery (RCA)thrombotic total occlusion, mid left anterior descending (LAD) artery thrombotic subtotal occlusion]. Left circumflex artery did not present with any significant obstruction. Left ventricular function was severely depressed with an ejection fraction of 25 %.
The patient underwent successful percutaneous intervention of RCA and LAD with stent placement. An intraaortic balloon pump was inserted for hemodynamic support.
Five days following the coronary intervention, while recovering in the hospital, the patient became hemodynamically unstable and developed respiratory distress requiring emergent intubation. At auscultation, a loud systolic murmur of mitral regurgitation was audible at the apex.


Echocardiography:

Transesophageal echocardiography showed Type II mitral valve dysfunction due to papillary muscle rupture. The prolapse of the anterior leaflet was clearly visible as shown here. On Doppler echocardiography the jet was posteriorly directed. The ruptured segment of the muscle could be directly viewed as a mobile ventricular mass. There was severe mitral valve regurgitation. The overall left ventricular systolic function was preserved.

Operative Procedure:
The patient was taken emergently to the operating room for mitral valve surgery. Following the exposure of the mitral valve, a detailed mitral valve analysis was performed and showed a prolapse of theA3 segment and the postero-medial commissure. The inspection of the left ventricle showed an extensive subendocardial hemorrhagic plaque involving the posterolateral wall. The examination of subvalvular apparatus showed a postero-medial papillary muscle with two heads. There was a complete rupture of the head which was supporting the anterior leaflet. The muscle was hemorrhagic, necrotic and very friable. The posterior head with chordae attachment to the posterior leaflet was intact. These anatomic findings were in accordance with echocardiographic findings of anterior leaflet prolapse.
The patient underwent a biologic mitral valve replacement with the preservation of the posterior leaflet. Postbypass transesophageal echocardiography showed a well-functioning bioprosthetic valve in the mitral position. Left ventricular function was mildly depressed.

Mitral Disease

Echocardiography is the key diagnostic tool used for determination of rheumatic valvular disease. Carpentier's type IIIa is the most common dysfunction seen in patients with rheumatic mitral valve. The characteristic lesions are commissural fusion with or without calcification, leaflet thickening / retraction, and chordae fusion and shortening. The hemodynamic consequence of this valvular dysfunction is mitral regurgitation associated with varying degrees of mitral stenosis.

Type IIIa dysfunction of the posterior leaflet associated with limited prolapse of the anterior leaflet (mostly A2 segment) is very characteristic of rheumatic mitral valve disease.

The presence of associated valvular lesions involving the aortic and tricuspid valves is strongly in favor of rheumatic etiology of valvular heart disease.
Echocardiography is also critical in assessing the mobility of the anterior leaflet, the extent of subvalvular apparatus lesions, and the presence and the extent of valvular calcification as they all predict the feasibility of valve reconstruction.

Finally, echocardiography is used to obtain quantitative measures such as mitral valve orifice area applying the continuity equation. Transvalvular peak and mean gradients are calculated with continuous-wave and pulsed-Doppler echocardiography using the modified Bernoulli equation. In patients with mitral stenosis and minimal symptoms, it is important to calculate transvalvular gradient at rest and during exercise.

Rheumatic Valve Disease

During the second half of the 20th century the improvement in the socio-economic situation and the widespread use of antibiotics led to the eradication of rheumatic fever in developed countries. In contrast, the incidence of this disease has remained extremely high in non-industrialized countries. Today, rheumatic fever still remains the principle cause of valvular heart disease and particularly mitral valve disease worldwide.As discussed extensively in the historic review section, a history of untreated group A Beta hemolytic streptococcal pharyngitis is the event that may lead to rheumatic fever. In this scenario, the rate of development of rheumatic fever is about 3%.The two major factors that should be considered regarding the risk of rheumatic fever are: 1) the intensity of the immune response during the episode of streptococcal pharyngitis and 2) the persistence of the organism during the recovery. The strain of Group A streptococcus also plays a role as M-types are associated with strong immune response. These so-called rheumatogenic strains have a cell wall which contains M proteins that are highly antigenic. The immunologic response to M proteins produces antibodies that may cross react with cardiac myosin. They also cross react with perivascular connective tissue leading to the formation of Aschoff bodies. It has also been suggested that cell-mediated immunity plays a definite role in the constitution of acute rheumatic valvular lesions. Jones Criteria, first described in 1944 and updated in 1992, remain relevant and are used for the diagnosis of initial attacks of rheumatic fever. They are divided into two categories of major and minor criteria. During the acute phase, carditis is noted in about 50% of patients. As mentioned first by Bouillaud, cardiac involvement is a pancarditis and acute valvulitis involving the left-sided valves is a characteristic feature of this disease. Mitral valve regurgitation due to type I dysfunction with annular dilatation is a hallmark of acute rheumatic carditis. With the resolution of the acute phase, the long-term prognosis is dominated by the extent and the progression of valvular heart disease.During the chronic phase, in patients with valvular manifestations but with no known history of rheumatic fever or untreated streptococcal pharyngitis, it may be difficult to establish the rheumatic origin of their valve disease. Echocardiography and intraoperative valve analysis may demonstrate characteristic lesions which would confirm this etiology.

Chronologic Approach

Chronologic approach the development of knowledge of the structure and function of the heart, circulatory system and subsequently the diseases of the heart with a particular emphasis on the mitral valve. In this section we analyze the work of major contributors from the European Renaissance until the end of the 19th century. Briefly, the 16th century can be viewed as the century of descriptional anatomy.

The development of the science of experimental physiology with the discovery of blood circulation took place in the 17th century. During that era, the science of histology was established and microscopic observation played a critical role in our understanding of the physiology of the circulation.The first pathological reports appeared toward the turn of this century with description of ossification of the cardiac valves . The 18th century witnessed the birth of anatomo-pathology and a great emphasis was placed on the correlation of clinical symptoms with autopsy findings. Finally, during the first half of the 19 century, great progress was made in physical diagnosis with the broader application of percussion and the invention of stethoscope.

Mitral Valve, Mitral Valve Repair, Mitral Valve Prolapse, Mitral Leakage, Mitral Disease, Mitral Valve Replacement, Farzan Filsoufi